Lesson 16

Atherosclerosis, microscopic

This high-magnifiation view of the necrotic center of an aortic atheroma shows foam cells and cholesterol clefts. In the process of atheroma formation, endothelial injury leads to increased permeability, leukocyte adhesion, and release of cytokines that attract blood monocytes, which become macrophages that accumulate lipids, becoming foam cells. Macrophages readily ingest oxidized LDL cholesterol through their scavenger receptors. Macrophages also generate cytokines driving cellular recruitment. An increased serum LDL level increases the amount of oxidized LDL, promoting this process. In contrast, HDL cholesterol tends to promote mobilization of lipid in an atheroma and transport to the liver.

Atherosclerosis, microscopic

This coronary artery cross-section shows severe occlusive atherosclerosis. The atheromatous plaque is circumferential and markedly narrows the remaining lumen. Note the prominent cholesterol clefts within this atheroma. This advanced atheromatous process involves the arterial media and the overlying intima with numerous cholesterol clefts. The remaining lumen has become occluded by a recent thrombus that fils it. Thrombosis is often the basis for acute coronary syndromes, including unstable angina, sudden death, and acute myocardial infarction.

Atherosclerosis, microscopic

This coronary artery cross-section shows residual smooth muscle in the media with overlying atheroma composed of extensive lipid deposition in lipophages and a cholesterol cleft from breakdown of those cells. Such plaques are prone to rupture, hemorrhage, and thrombosis. Platelets become activated and adhere to sites of endothelial injury, then release cytokines such as platelet-derived growth factor that promote smooth muscle proliferation, and the adherent platelet mass increases the size of the plaque while narrowing the residual arterial lumen. Use of antiplatelet agents such as aspirin helps reduce platelet “stickiness” and slows platelet participation in atheroma formation. Daily exercise is even better.

Aortic aneurysm, gross

Atherosclerosis involving the intima and media may focally weaken the wall of the aorta so that it bulges out to form an aneurysm. A classic atherosclerotic aortic aneurysm typically occurs in the abdominal portion distal to the renal arteries, as shown here. Aortic aneurysms tend to enlarge over time, and those with a diameter greater than 5 to 7 cm are more likely to rupture. Aneurysms may also form in the larger arterial branches of the aorta, most often the iliac arteries. On physical examination, there may be a palpable pulsatile abdominal mass with an atherosclerotic aortic aneurysm. Increased expression of matrix metalloproteinases that degrade extracellular matrix components such as collagen is observed in aortic aneurysms.

Aortic aneurysm, gross

This aorta has been sectioned longitudinally to reveal a large abdominal atherosclerotic aortic aneurysm distal to the renal arteries (at the right) and proximal to the iliac bifurcation (at the left). This bulging aneurysm, 6 cm in diameter, is filed with abundant layered mural thrombus. Note the rough atheromatous surface of the aortic lumen.

Hyaline arteriolosclerosis, microscopic

Another form of arteriosclerosis (hardening of the arteries) in addition to atherosclerosis is hyaline arteriolosclerosis, typically seen in kidneys and brain. It is shown here involving the markedly thickened arteriole at the lower right of this glomerulus with PAS stain. This change often accompanies benign nephrosclerosis, leading to progressive loss of nephrons and eventual renal atrophy. Hyaline arteriolosclerosis is also seen in elderly individuals, who are often normotensive. More advanced arteriosclerotic lesions may occur in persons with diabetes mellitus or hypertension.

Medial calcific sclerosis, microscopic

Mönckeberg medial calcifi sclerosis is the most insignifiant form of arteriosclerosis (atherosclerosis and arteriolosclerosis are signifiant because of arterial luminal narrowing). It is more common in the elderly. Note the purplish blue calcifiations involving only the media; the lumen appears unaffected by this process. No signifiant clinical consequences occur in most patients, and it is usually an incidental fiding. Recall this process when you see calcifid muscular arteries on a radiograph of the pelvic region, although other regions such as the neck or breast may also be involved.

Aortic dissection, microscopic

The tear in this aorta extends through the media, but blood also dissects along the media. Medical management can be undertaken; but with leakage or rupture, surgical repair of the dissection can be performed with closure of the tear and placement of a synthetic graft or endovascular stent.

Aortic dissection, gross

This aorta opened longitudinally shows an area in the thoracic portion of limited dissection that is organizing within the media. The red-brown thrombus can be seen on both sides of the section as it extends around the aorta. The intimal tear would have been at the left. This creates a “double lumen” to the aorta. This aorta shows severe atherosclerosis, which was the major risk factor for dissection in this patient.